Publisher Health

Predicting sudden cardiac death, and perhaps even addressing a person’s risk to prevent future death, may be possible through artificial intelligence (AI) and could offer a new move toward prevention and global health strategies, according to preliminary research to be presented at the American Heart Association’s Resuscitation Science Symposium 2023. The meeting, Nov. 11-12, in Philadelphia is a premier global exchange of the most recent advances related to treating cardiopulmonary arrest and life-threatening traumatic injury.
“Sudden cardiac death, a public health burden, represents 10% to 20% of overall deaths. Predicting it is difficult, and the usual approaches fail to identify high-risk people, particularly at an individual level,” said Xavier Jouven, M.D., Ph.D., the lead author of the study and professor of cardiology and epidemiology at the Paris Cardiovascular Research Center, Inserm U970-University of Paris. “We proposed a new approach not restricted to the usual cardiovascular risk factors but encompassing all medical information available in electronic health records.”
The research team analyzed medical information with AI from registries and databases in Paris, France and Seattle for 25,000 people who had died from sudden cardiac arrest and 70,000 people from the general population, with data from the two groups matched by age, sex and residential area. The data, which represented more than 1 million hospital diagnoses and 10 million medication prescriptions, was gathered from medical records up to ten years prior to each death. Using AI to analyze the data, researchers built nearly 25,000 equations with personalized health factors used to identify those people who were at very high risk of sudden cardiac death. Additionally, they developed a customized risk profile for each of the individuals in the study.
The personalized risk equations included a person’s medical details, such as treatment for high blood pressure and history of heart disease, as well as mental and behavioral disorders including alcohol abuse. The analysis identified those factors most likely to decrease or increase the risk of sudden cardiac death at a particular percentage and time frame, for example, 89% risk of sudden cardiac death within three months.
The AI analysis was able to identify people who had more than 90% of risk to die suddenly, and they represented more than one fourth of all cases of sudden cardiac death.
“We have been working for almost 30 years in the field of sudden cardiac death prediction, however, we did not expect to reach such a high level of accuracy. We also discovered that the personalized risk factors are very different between the participants and are often issued from different medical fields (a mix of neurological, psychiatric, metabolic and cardiovascular data) — a picture difficult to catch for the medical eyes and brain of a specialist in one given field” said Jouven, who is also founder of the Paris Sudden Death Expertise Center. “While doctors have efficient treatments such as correction of risk factors, specific medications and implantable defibrillators, the use of AI is necessary to detect in a given subject a succession of medical information registered over the years that will form a trajectory associated with an increased risk of sudden cardiac death. We hope that with a personalized list of risk factors, patients will be able to work with their clinicians to reduce those risk factors and ultimately decrease the potential for sudden cardiac death.”
Among the study’s limitations are the potential use of the prediction models beyond this research. In addition, the medical data collected in electronic health records sometimes include proxies instead of raw data, and the data collected may be different among countries, requiring an adaptation of the prediction models.

People who have a higher biological age than their actual chronological age have a significantly increased risk of stroke and dementia, especially vascular dementia. These are the results of a study from Karolinska Institutet in Sweden published in the Journal of Neurology, Neurosurgery and Psychiatry.
The study, which was led by Sara Hägg, associate professor, and Jonathan Mak, doctoral student at the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, shows that the increased risk persists even if other risk factors such as genetics, lifestyle and socioeconomics are taken into account.
As we age, the risk of chronic diseases such as cancer, cardiovascular disease and neurodegenerative disorders increases. Researchers have traditionally relied on chronological age — the number of years a person has been alive — as an approximate measure of biological age.
“But because people age at different rates, chronological age is a rather imprecise measure,” says Sara Hägg.
In order to measure biological age and the link to disease, the researchers used data from the UK Biobank. They studied a cohort of 325,000 people who were all between 40 and 70 years old at the time of the first measurement.
Biological age was calculated using 18 biomarkers, including blood lipids, blood sugar, blood pressure, lung function and BMI. The researchers then investigated the relationship between these biomarkers and the risk of developing neurodegenerative diseases such as dementia, stroke, ALS and Parkinson’s disease within a nine-year period.
When compared to actual, chronological age, high biological age was linked to a significantly increased risk of dementia, especially vascular dementia, and ischemic stroke, (i.e. blood clot in the brain).

World Rugby Chairman Sir Bill Beaumont has welcomed results from the largest ever studies into the forces experienced by rugby players. The results, which provide players and parents with greater clarity and confidence than ever before into the benefits and safety of rugby, are a first anywhere in world sport.
The Otago Community Head Impact Detection study (ORCHID) a joint project between World Rugby, Prevent Biometrics, New Zealand Rugby, Otago Rugby and the University of Otago, has published the first independent, peer-reviewed findings into community rugby following almost two years of trail-blazing research. The study measures over 17,000 separate head acceleration events across more than 300 players from senior rugby through to U13s level.
This work was followed by the Elite Extension of the ORCHID study in partnership with the Ulster University and Premiership Rugby. Further updates into the women’s community game are currently being prepared for peer review and publication.
Both studies used smart mouthguard technology, supplied by Prevent Biometrics, to understand the forces on the head experienced by players both in matches and training situations. The mouthguards measure g-forces which are experienced for less time than it takes to blink, using technology independently verified both in research laboratories and on the field of play.
The ORCHID paper shows that in the men’s community game: 86 per cent of forces measured are the same as or less than those experienced in other forms of exercise such as running, jumping or skipping 94 per cent of forces are lower than those previously measured on people riding a rollercoaster The large majority of events resulting in the highest measured forces are as a result of poor technique in the tackle and at the breakdownThe Elite Extension study also showed that: Most contact events in elite rugby do not result in any significant force to the head. Where low, medium and high force events do occur they are most common in tackles and carries, followed by rucks Both men’s and women’s forwards were more likely to experience force events than backsWorld Rugby has already used preliminary findings from the ORCHID study to inform trials of a lower tackle height in the community game. The international federation has also expanded and enhanced the range of training for players and coaches available for free online including the Tackle Ready and new Breakdown Ready programmes.

Men who are overweight or obese at age 18 have a higher risk of 17 different cancers later in life. This has been shown in a study at the University of Gothenburg. The research also describes how the youth obesity epidemic is expected to affect the cancer situation over the next 30 years.
In August, a study on higher cancer risk in men who had lower aerobic fitness recorded at the time of compulsory conscription for military service at the age of 18 was presented. The results were independent of any overweight or obesity at conscription.
In two new studies published in the journals Obesity and Cancer Medicine, the same research team is now focusing on body mass index (BMI), while the results are independent of the participants’ aerobic fitness level. And it turns out that higher BMI at age 18 can be linked to even more cancers later in life than poor fitness at the same age.
High BMI at conscription was associated with a higher risk of 17 cancers: lung, head and neck, brain, thyroid, esophageal, stomach, pancreatic, liver, colon, rectal, kidney, and bladder cancer, as well as malignant melanoma, leukemia, myeloma, and lymphoma (both Hodgkin’s and non-Hodgkin’s).
Higher risk already at “normal” BMI
For several of the cancer types, the risk was elevated already at a BMI of 20-22.4, within the usually used range of normal weight (18.5-24.9). These included cancers of the head and neck, esophagus, stomach, pancreas, liver, and kidney, as well as malignant melanoma and non-Hodgkin’s lymphoma.
“This suggests that the current definition of normal weight may be applicable primarily for older adults, while an optimal weight as a young adult is likely to be in a lower range. Our research group has drawn similar conclusions regarding BMI in early adulthood and later cardiovascular disease,” says Maria Åberg, professor of family medicine at Sahlgrenska Academy at the University of Gothenburg and senior author.

A speech prosthetic developed by a collaborative team of Duke neuroscientists, neurosurgeons, and engineers can translate a person’s brain signals into what they’re trying to say.
Appearing Nov. 6 in the journal Nature Communications, the new technology might one day help people unable to talk due to neurological disorders regain the ability to communicate through a brain-computer interface.
“There are many patients who suffer from debilitating motor disorders, like ALS (amyotrophic lateral sclerosis) or locked-in syndrome, that can impair their ability to speak,” said Gregory Cogan, Ph.D., a professor of neurology at Duke University’s School of Medicine and one of the lead researchers involved in the project. “But the current tools available to allow them to communicate are generally very slow and cumbersome.”
Imagine listening to an audiobook at half-speed. That’s the best speech decoding rate currently available, which clocks in at about 78 words per minute. People, however, speak around 150 words per minute.
The lag between spoken and decoded speech rates is partially due the relatively few brain activity sensors that can be fused onto a paper-thin piece of material that lays atop the surface of the brain. Fewer sensors provide less decipherable information to decode.
To improve on past limitations, Cogan teamed up with fellow Duke Institute for Brain Sciences faculty member Jonathan Viventi, Ph.D., whose biomedical engineering lab specializes in making high-density, ultra-thin, and flexible brain sensors.
For this project, Viventi and his team packed an impressive 256 microscopic brain sensors onto a postage stamp-sized piece of flexible, medical-grade plastic. Neurons just a grain of sand apart can have wildly different activity patterns when coordinating speech, so it’s necessary to distinguish signals from neighboring brain cells to help make accurate predictions about intended speech.

Drinking water with high levels of nitrate is a global problem linked to a variety of health problems including birth defects and cancer. For example, there is a growing body of scientific evidence to support that nitrate in drinking water increases the risk of colorectal cancer — the third most common cancer worldwide and the second leading cause of cancer-related deaths, according to WHO.
Studies suggest that the nitrate levels in drinking water will increase in a number of countries around the world especially with increased nitrogen application and economic growth.
Denmark follows the EU limit of no more than 50 milligrams of nitrate per liter of water. Even though concentrations are well below this ceiling across much of Denmark, amounts of nitrate in drinking water are significant enough to increase the risk of developing colorectal cancer in several areas. A large Danish population-based cohort study from 2018 and several international studies have demonstrated this.
A new study by researchers from the University of Copenhagen, Aarhus University and the Geological Survey of Denmark and Greenland (GEUS) demonstrates that Danish society could save more than $300 million a year by reducing nitrate concentrations in drinking water and avoid 127 cases of colorectal cancer annually.
“The EU requirement of no more than 50 milligrams of nitrate per liter of water is a minimum requirement, so we could easily establish stricter requirements in Denmark. Our research shows that this would benefit public health, and at the same time, save society a lot of money,” says Brian H. Jacobsen, senior researcher at the Department of Food and Resource Economics at the University of Copenhagen.
Jacobsen is the lead author of the new study, now published in the journal Science of the Total Environment.
Benefits far exceed costs
A Danish population-based study from 2018 shows a statistically significant correlation with an increased risk of colorectal cancer when nitrate levels in drinking water exceed approximately 4 mg/L and an even higher risk when above approximately 9 mg/L.

Researchers have identified a new neural circuit in the brain which produces a strong sense of discomfort when activated. The discovery also allows them to show for the first time that the subthalamic nucleus, a structure in the brain that controls voluntary movements, may also play a role in the development of depression. The results could lead to better treatments for Parkinson’s disease. The study has been published in the scientific journal Cell Reports.
“Our study shows that a specific region of the brain is involved in aversion and avoidance behaviour when stimulated. We’ve studied how mice behave when the subthalamic nucleus is activated using optogenetic stimulation,” explains Åsa Mackenzie, Professor at the Department of Organismal Biology at Uppsala University, and the lead author of the study.
The research team has previously discovered that mice whose subthalamus is activated seek to get away from the stimulation. In the new study, they were able to show that this behaviour is linked to aversion and that the avoidance behaviour not only takes place while the subthalamic nucleus is activated, but also that the discomfort lingers in the memory. When the mice were placed in the same environment at a later time, they showed an equally strong avoidance behaviour even though the stimulation was now deactivated. The associations were thus strong enough to sustain the behaviour.
Aversion is the opposite of reward and plays an important role in making us avoid things that make us feel bad. In humans, it is known that strong activation of the brain’s aversion system can lead to depression.
In the new study, the researchers have not only discovered the location in the brain in which the aversion occurs, but have also identified neural circuits originating in the subthalamic nucleus that connect directly to the brain’s emotional system, which becomes active during strong feelings of discomfort.
“That the subthalamus gives rise to aversion and avoidance behaviour is an important finding for two main reasons. It increases our understanding of the brain’s emotional system and how brain activity can lead to psychiatric symptoms such as depression and apathy. Secondly, it may explain why people with Parkinson’s disease treated with deep brain stimulation (DBS) can experience these kinds of side effects,” continues Mackenzie.
In Parkinson’s disease, the subthalamus is overly active, but stimulating this brain region in severely ill Parkinson’s patients using DBS with implanted electrodes ‘corrects’ this and eliminates tremors and other motor problems. The treatment often works very well. However, some patients experience side effects such as severe depression.

Domestic cats introduced from the Near East and wildcats native to Europe did not mix until the 1960s, despite being exposed to each other for 2,000 years, according to two research papers published today in Current Biology.
An international team has found new archaeological and genetic evidence which transforms our understanding of the history of cats in Europe. The team sequenced and analysed both wild and domestic cats, including 48 modern individuals and 258 ancient samples excavated from 85 archaeological sites over the last 8,500 years. They then assessed the patterns of hybridisation after domestic cats were introduced to Europe over 2,000 years ago and came into contact with native European wildcats.
The results of the studies demonstrate that, since their introduction, domestic cats and European wildcats generally avoided mating. About 50 years ago in Scotland, however, that all changed. Perhaps as a result of dwindling wildcat populations and a lack of opportunity to mate with other wildcats, rates of interbreeding between wild and domestic cats rose rapidly.
Jo Howard-McCombe from the University of Bristol and the Royal Zoological Society of Scotland explains, ‘Wildcats and domestic cats have only hybridised very recently. It is clear that hybridisation is a result of modern threats common to many of our native species. Habitat loss and persecution have pushed wildcats to the brink of extinction in Britain. It is fascinating that we can use genetic data to look back at their population history, and use what we have learnt to protect Scottish Wildcats.’
Professor Greger Larson, from the University of Oxford, says, ‘We tend to think of cats and dogs as very different. Our data suggests that, at least with respect to avoiding interbreeding with their wild counterparts, dogs and cats are much more similar to each other than they are to all other domestic animals. Understanding why this is true will be fun to explore.’
Professor Mark Beaumont, from the University of Bristol, adds, ‘The nature of the Scottish wildcat and its relation to feral domestic cats has long been a mystery. Modern molecular methods and mathematical modelling have helped to provide an understanding of what the Scottish wildcat truly is, and the threats that have led to its decline.”‘
Domestic animals including cattle, sheep, goats, dogs, and pigs have been closely associated with people since the emergence of farming communities more than 10,000 years ago. These tight relationships led to the human-mediated dispersal of plants and animals well beyond their native ranges.
Over the last decade, genomic sequences of modern and ancient individuals have revealed that, as domestic animals moved into new regions, they interbred with closely related wild species, which has dramatically altered their genomes. This pattern has been seen in every domestic animal, except dogs. It would be fascinating to know whether domestic cats interbred with European wildcats, but the decline of native wildcat populations across Europe, and the lack of ancient cat genomes has made it difficult to do so.
The two studies, were carried out at universities in Munich, Bristol, Oxford and the Royal Zoological Society of Scotland.

This huge step forward in understanding how neurons communicate through extremely short proteins called neuropeptides will help scientists understand how our emotions and mental states are controlled, as well as widespread neuropsychiatric conditions like eating disorders, OCD and PSTD.
The map, which details 31,479 neuropeptide interactions between the worm’s 302 neurons, shows where each neuropeptide, as well as each receptor for those peptides, acts in the animal’s nervous system. Neuropeptides allow communication between neurons that are not immediately next to each other, so their networks can be thought of as a wireless connectome. A connectome is a map of the neurons which make up an organism’s brain and the detailed circuitry of neural pathways within it.
Researchers are making rapid progress in building connectomes for simple organisms, but until now, no-one had managed to build a map of a neuropeptide network in any animal.
Dr William Schafer and PhD student, Lidia Ripoll-Sánchez, both of the Medical Research Council Laboratory of Molecular Biology in Cambridge in the UK, led the work, together with Petra Vértes of Cambridge University and Isabel Beets from KU Leuven in Belgium. Their study is published in Neuron today.
The worm they studied is called C. elegans. It’s harmless, around 1mm long, and lives in soil. C. elegans has a very simple anatomy, but it shares many of the essential biological characteristics that are central problems of human biology.
Dr Schafer said:
“Neuropeptides and their receptors are among the hottest new targets for neuroactive drugs. For example, the diabetes and obesity drug Wegovy targets the receptor for the peptide GLP-1. But the way these drugs act in the brain at the network level is not well-understood.

Multiple sclerosis patients whose blood tests reveal elevated NfL, a biomarker of nerve damage, could see worsening disability one to two years later, according to a new study spearheaded by researchers at UC San Francisco.
The study is the first to quantify the timeframe preceding disability worsening in which injury to the central nervous system takes place, said co-first author Ahmed Abdelhak, MD, of the UCSF Department of Neurology and the Weill Institute for Neurosciences.
Almost 1 million Americans suffer from MS. In advanced cases, patients may have limited mobility and experience spasticity, weakness, poor coordination and incontinence. However, recent advances suggest that more severe symptoms can be substantially delayed or even averted.
“This rising of NfL up to two years before signs of disability worsening, represents the window when interventions may prevent worsening,” said Abdelhak.
In the study, publishing in JAMA Neurology on Nov. 6, 2023, and co-led by University Hospital and University of Basel, in Switzerland, the researchers looked at the incidence of disability worsening, defined as six months or more of increased impairment reflected in a higher score on the Expanded Disability Status Scale. They distinguished between disability worsening with relapse, which involves residual symptoms or the return of old ones following relapse, and gradual progression of symptoms without relapse.
91% at elevated risk of developing disability worsening
The researchers tracked data spanning a 10-year period from approximately 4,000 patient visits to UCSF, comprising the EPIC study, and from approximately 9,000 patient visits to multiple sites in Switzerland, comprising the SMSC study. Together, the two studies included almost 1,900 patients. Among those, 570 patients were identified with disability that continued to worsen, of which the majority were independent of relapses.